Subarachnoid haemorrhage (SAH) is an acute cerebrovascular disease usually triggered by rupture of a cerebral aneurysm, resulting in blood leakage into the subarachnoid space. Although SAH accounts for only 5% of strokes, its high lethality and disability make it a major health problem.The acute phase of SAH is lethal in up to 50% of cases, and approximately 30-40% of survivors will face severe neurological impairments, such as cognitive, motor, and affective deficits. Oxidative stress plays a key role in secondary brain damage after SAH, where excess reactive oxygen species (ROS) damage cells, triggering blood-brain barrier disruption, brain oedema and neuronal damage. Neuroglobin (Ngb), as a neuroprotective factor, can exert significant neuroprotective effects by scavenging ROS, regulating the antioxidant enzyme system, and inhibiting mitochondria-mediated apoptosis.Ngb also plays an important role in the maintenance of mitochondrial function, the promotion of ATP production, and the ?enhancement of cellular antioxidant capacity, which can effectively alleviate the damage of oxidative stress on the nervous system. An in-depth study of the role of NGB in oxidative stress after SAH, revealing its mechanism of regulating ROS scavenging and antioxidant enzyme activity, has important theoretical significance and clinical application value, and provides a scientific basis for the development of NGB-based therapeutic strategies to improve the prognosis of SAH patients. |